Effects of tourniquet ischemia and postischemic edema on muscle metabolism.

In vivo interstitial muscle pressures measured by wick catheter, tissue gas tensions measured by mass spectrometer, and glucose and high-energy phosphate metabolism measured fluorometrically were studied in the anterior tibial (AT) and vastus lateralis (VL) muscles of primate limbs during and following tourniquet ischemia (2.5 hours; 400 mm Hg) to elucidate postischemic edema and its metabolic consequences. During ischemia, interstitial pressure in the VL rose, while in the AT it decreased, but 24 hours later pressures in both experimental muscles were significantly greater than those in the controls. In both experimental muscles PO2 decreased significantly within 15 minutes of ischemia. PCO2 increased significantly in the AT at 30 minutes and at 75 minutes in the VL muscle. Twenty-four hours later only PO2 in the experimental AT was significantly different than its matched control. During ischemia glucose and phosphocreatine (CrP) decreased significantly, and G-6-P and lactate increased significantly in both muscles, but at 24 hours glucose levels were 25% lower and G-6-P 16.2% higher in the experimental AT and CrP 34% lower in the experimental VL. This study shows that there are significant acute and delayed alterations in primate muscle metabolism following tourniquet ischemia and suggests that these changes may be related to the anatomic location of the muscle studied and the type of trauma it has sustained.